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MHD > Thyroid > Flashcards

Thyroid Flashcards

1
Q

What are follicles lined by?

A

cuboidal to low columnar follicular cells

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2
Q

What do parafollicular or C cells secrete? What origin ar they?

A

calcitonin-promotes absorption of calcium by the skeletal system and inhibits reabsorption of bone
Neural crest origin

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3
Q

What is the mechanism of action and function of thyroid hormones?

A
  1. Stimulation of protein synthesis
  2. Up regulation of carbohydrates and lipid catabolism
  3. Increase in basal metabolic rate
  4. critical role in the development of brain in fetuses and neonates
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4
Q

Thyrotoxicosis

A

Hyper metabolic state due to increased circulating levels of thyroid hormones (T4 and T3)
-most commonly caused by hyper functioning of the thyroid gland but can be not associated with hyperthyroidism

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5
Q

Clinical manifestations of hyperthyroidism/ thyrotoxicosis

A

Excess thyroid hormone and over activity of sympathetic nervous system

  1. Increased BMR-soft warm flushed skin
  2. Heat intolerance and excess sweating
  3. Weight loss despite increased appetite
  4. Cardiovascular-increased CO, tachy, palpitaitons, cardiomegaly, arrhythmias especially atrial fibrillation is common in the elderly
  5. Development of low output heart failure
  6. Neuromuscular-nervousness, emotional lability, insomnia, muscular weakness, fine tremor of the hands
  7. proximal muscle weakness and decreased muscle mass
  8. Gastrointestinal: hypermotility, malabsorption
  9. Wide staring gaze and lid lag
  10. Thyroid ophthalmopathy (proptosis) only associated with graves
  11. Stimulates bone resorption and osteoporosis
  12. THyroid storm-medical emergency
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6
Q

Diagnosis of hyperthyroidism

A

TSH levels-usually decreased-Most sensitive

Free T4-usually increased

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7
Q

How do you exclude secondary or pituitary associated hyperthyroidism?

A

TRH stimulation test

  • inject TRH
  • if normal rise in TSH then it is not secondary hyperthyroidism
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8
Q

What radioactive iodine uptake results indicate Graves, toxic adenoma, or thyroiditis?

A

graves: diffuse uptake
toxic adenoma: localized
thyroiditis: reduced uptake

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9
Q

What is the most common cause of hypothyroidism?

A

primary hypothyroidism

-can be accompanied by enlargement of the gland(goiter)

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10
Q

What is the most common worldwide congenital hypothyroidism due to?

A

iodine deficiency

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11
Q

Cretinism

A

Hypothyroidism in infants or early childhood

  • secondary to iodine deficiency or rarely from inborn errors in metabolism
  • impaired development of skeletal muscles and CNS: severity varies to timing of deficiency
  • if maternal thyroid hormone deficiency before development of fetal thyroid, mental retardation is sever
  • mental retardation, short stature, coarse facial features
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12
Q

Hypothyroidism Myxedema

A

Adult hypothyroidism
Gradual slowing of mental and physical activity
-fatigue, lethargy, apathy, slowed speech
-cold intolerance and reduced sweating
-overweight and constipation
-periorbital edema, thick coarse skin, enlarged tongue (deposition of glycosaminoglycans)
-reduced cardiac output causes shortness of breath and decreased exercise capacity
-promotes an atherogenic profile (increased cholesterol)-adverse cardiovascular mortalities

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13
Q

What lab values do you find in hypothyroidism?

A

Decreased T4
TSH levels-most sensitive for hypothyroidism
Primary-Increased TSH
Secondary-Decreased/normal TSH

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14
Q

Thyroiditis

types with Pain and No pain

A
  1. Inflammation with pain, sometimes severe
    - Infectious thyroiditis
    - subacute granulomatous thyroiditis (De quervain thyroiditis)
  2. Relatively little pain
    - Subacute lymphocytic thyroiditis
    - Riedel’s thyroiditis
    - Hashimoto’s thyroiditis
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15
Q

Hashimoto Thyroiditis

A

most common hypothyroidism in non-iodine deficient areas

  • autoimmune destruction of thyroid gland
  • 45-65
  • major cause of non endemic goiter in pediatric age group
  • strong genetic component
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16
Q

What are the three mechanisms of breakdown in self tolerance and induction of thyroid autoimmunity in Hash?

A
  1. T cell mediated cytotoxicity-CD8
  2. Thyrocyte injury-CD4-INF gamma-macrophages
  3. Antibody-dependent cell mediated cytotoxicity
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17
Q

What antibodies are seen in hashimoto thyroiditis?

A
  1. Thyroglobulin and thyroid peroxidase (TPO)!!!
  2. TSH receptor
  3. Iodine receptor
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18
Q

Hashimoto thyroiditis
Gross
Histology

A 
Gross
Diffusely enlarged gland 
Intact Capsule 
Well demarcated 
Pale, yellow, tan and somewhat nodular and firm

Histology:

  1. Thyroid follicles lined by Hurthle cells/oncocytes
    - have abundant granular pink cytoplasm (numerous mitochondria)
  2. formation of germinal centers
  3. Thyroid parenchyma infiltrated by mononuclear inflammatory cells
    - blue lymphocytes
    - pink cells forming a follicle with colloid in the middle-residual follicular cells
19
Q

Clinical course Hashimoto Thyroiditis

A
  • transient hyperthyroidism due to disruption of thyroid follicles with release of thyroid hormones (hashitoxicosis)
  • gradual hypothyroidism
  • increased risk of developing other autoimmune
  • increased risk of developing Non Hodgkin B cell lymphoma
20
Q

Subacute/Granulomatous (de quervain) thyroiditis

A

40-50 years of age

  • viral or post-viral inflammatory response
  • viral antigens or virus induced host tissue damage stimulates formation of cytotoxic T cells which then damage the thyroid follicular cells (process is self limited)
  • Most Common cause of thyroid pain
  • variable enlargement of thyroid
  • history of upper respiratory infection
  • transient hyperthyroidism–hypothyroidism–euthyroid
  • hyperthyroid phase: T3, T4, decreased TSH, radioactive iodine is diminished
  • recovery and normal thyroid function in 6-8 weeks
21
Q

Subacute/Granulomatous (de quervain) thyroiditis

histology

A
  1. unilateral or bilateral enlarged firm with intact capsule
  2. changes are patchy
    3.
    early stage-disruption of follicles with collections of neutrophils forming microabscesses
    later stage-aggregates of lymphocytes, plasma cells and activated macrophages around damaged thyroid follicles
    -multinucleated giant cells of enclosed fragments of colloid
  3. eventually chronic inflammation and fibrosis
22
Q

Riedel thyroiditis

A

rare disorder of unknown etiology

  • extensive fibrosis involving the thyroid and contiguous neck structures
  • hard and fixed mass-clinically simulating cancer**
  • may be associated with idiopathic fibrosis at other sites like retroperitoneum
  • presence of circulating antibodies- autoimmune etiology
23
Q

Graves Disease

A

Most common cause of hyperthyroidism

  1. Hyperthyroidism due to diffuse hyperfunctional enlargement of thyroid
  2. infiltrative opthalmo exophthalmo-accumulation of loose connective tissue behind eyeballs-weak extraocular muscles
  3. infiltrative dermopathy pretibial myxedema (present in minority of patients)
  • 20-40 yrs
  • 30-40% concordance in monozygotic twins as compared to 5% in di
24
Q

What are the autoantibodies seen in graves disease

A
  1. Thyroid stimulating immunoglobulin (TSI)-binds to TSH receptor and mimics its actions (specific for graves)
  2. Thyroid growth stimulating immunoglobulin-cause(TGI) proliferation of follicular epithelium
  3. TSH-binding inhibitor immunoglobulin (TBII)
25
Q

What does graves look like grossly and histologically

A

Gross
symmetrically enlarged glands
weigh may be >80 g
soft meaty appearance of the parenchyma

Histological:
Crowded and tall follicular cells
Formation of small papillae filling the lumen of the follicles
Papillae do NOT contain fibrovascular cords
Pale colloid with scalloped margins
-lymphoid infiltrate with germinal centers common

26
Q

What lab findings do you see with graves disease?

A

Increased serum levels of thyroid hormones
Decreased TSH
Increased radioactive iodine uptake with diffuse uptake on radioiodine scans

27
Q

What are the treatments to graves disease?

A
  1. Beta Blockers- symptomatic treatment of increased adrenergic tone (tachy, palp, tremulousness, anxiety)
  2. Propylthiouracil: decreased thyroid hormone synthesis
  3. radioiodine ablation
  4. surgery
28
Q

Diffuse/ Nontoxic simple goiter
Gross
HIsto
CLinical

A

Enlargement of the entire glad without producing nodularity
Diffuse symmetric enlargement

Gross
100-150 gm
cut surface-brown, glassy and translucent

Histologically:
2 phases
1. hyperplastic phage-enlarged thyroid gland with crowded follicular cells
2. colloid involution - some follicles are distended and some are small
-entire gland shows flattened epithelium and follicles filled with colloid

Clinical course

  • vast majority euthyroid
  • mass effect-large thyroid my press on trachea, esophagus and cosmetic disfigurement
  • Normal T4 and T3
  • Elevated TSH or in the upper limit of normal
29
Q

Multinodular Goiter
Gross
Histology
Clinical

A

Asymmetric enlargement with numerous nodules

  • evolvement from diffuse due to repeated episodes of hyperplasia and involution
  • older adults
  • both polyclonal and monoclonal nodules occur within the same gland
  • toxic or non toxic
Gross
Asymmetric multilobulated 
200 gm 
irregular nodules containing gelatinous colloid
foci of fibrosis and calcification

Histology
Colloid rich follicles lined by flattened inactive epithelium
-areas of follicular hyperplasia DO NOT have a prominent capsule between the hyperplastic nodule and adjacent parenchyma

30
Q

Multinodular Goiter clinical features? How do you tell if the mass is benign or malignant

A
  • Mass effect with disfigurement or compression
  • most patients euthyroid

-minority develop toxic due to development of -
autonomous nodule (plummer’s syndrome)
risk of malignancy

31
Q

Nodules more likely to be neoplastic in:

A 
90% 20 year survival
More likely to neoplastic:
-single nodule
-young patients
-male patients 
-nonfunctioning "cold" nodule
-history of radiation to the head the neck
32
Q

Follicular Adenoma
Mutation
Gross
Histology

A

Discrete solitary masses derived from follicular epithelium
Mutation:
RAS or PAX8-PPARG fusion gene
-similar to mutations seen in follicular carcinomas
Gross:
solitary, ENCAPSULATED, spherical mass
-well demarcated, 3cm
-gray-white to red brown mass
-may have areas of hemorrhage, necrosis or calcification
Histology:
neoplastic cells arranged in closely packed follicles
-well defined intact capsule (distinguish from hyperplastic nodules of multinodular goiter)
-uniform small follicles
hurthle cell/oxyphilic/oncocytic adenoma

33
Q

Follicular Adenoma

Clinical features

A
  • Capsule well defined and intact
  • NEED ENTIRE NODULE FOR DIAGNOSIS ***
Painless asymptomatic mass
cold on radioactive iodine scan
rarely functioning toxic adenoma
treatment lobectomy
excellent prognosis-do not recur or metastasize
34
Q

Are males or females more likely to get carcinomas of the thyroid in middle adulthood, what about in childhood and late adult life? What type of carcinoma is most common?

A

> F early middle adult
M=F childhood and late adult life
Papillary carcinoma

35
Q

Papillary Carcinoma

A

commonly 25-50yrs
majority associated with radiation exposure

gross:
solitary or multifocal lesion 
-may be well circumscribed and encapsulated or may be ill defined and infiltrative
-papillary structures
-foci of fibrosis and calcification

Histology:
Branching papillae with fibrovascular cores lined by multiple layers of cuboidal to columnar epithelium
**Diagnosis based on nuclear features
-longitudinal nuclear grooves
-ground glass or orphan annie eyed nuclei
-psammoma bodies-calcified lamellar concretions usually seen in the cores of the papillae

36
Q

Variants of Papillary carcinoma

A
  1. Follicular variant-based on nuclear features-frequently encapsulated, lower incidence of lymph node and extrathyroidal metastasis and favorable prognosis (no papillae seen)
  2. Tall variant-tall columnar cells with intense eosinophilic cytoplasm lining the papillary structures, aggressive behavior
  3. Diffuse sclerosis-younger individuals including kids
  4. Papillary microcarcinomas-less than 1cm
37
Q

Papillary Carcinoma clinical features

A
  • May be asymptomatic nodule or lymph node metastasis
  • cold

Diagnose:
diagnosed by fine needle aspiration cytology

Treat:
Total thyroidectomy with excision of abnormal appearing lymph nodes

Good prognosis>95% ten-year survival
prognosis dependent on: >40 less favorable, extrathyroid extension and distant metastasis (stage), isolated cervical lymph node met does not have effect on prognosis

38
Q

Papillary carcinoma genetic events

A
  1. Rearrangement of RET
    10q11 with RET/PTC translocation 20-40%
  2. Paracentric inversions or translocations of NTRK1 5-10%
  3. BRAF gene-adverse prognostic factors 33-50%
39
Q

Follicular Carcinoma

A

Second most common thyroid cancer
older age 40-60
Higher incidence in iodine deficient area
-minimally invasive or widely invasive

Gross:
-single well circumscribed nodule largely replacing almost the entire lobe
-nodule has light tan appearance and contain foci of hemorrhage
(may be difficult to distinguish from follicular adenomas grossly)
-may extend beyond capsule to involve adjacent neck structures

Histology:
lacks typical nuclear features of papillary carcinoma
-vascular invasion and/or capsular invasion

40
Q

Follicular Carcinoma clinical course/genetics

A
  • Slowly growing painless nodule
  • cold
  • hematogenous met to bone, lung, liver

Treatment:
total thyroidectomy with radioactive iodine

Prognosis dependent on metastasis

Genetics:
1/3 to 1/2 PI3K/AKT pathway
1/3 to 1/2 have translocation (2;3)(q13;p25) resulting in PAX8/PPARG fusion product

41
Q

Medullary Carcinoma

A

Neuroendocrine neoplasm derived from the parafollicular or C cells

  • may secrete calcitonin or ACTH or VIP
  • 70 % sporadic (single), 30% familial or associated with MEN2A or 2B (multiple)
  • MEN: first decade
  • Familial or sporadic: 4 or 5th decade

Gross:
solid grey tan tumor with NO well defined capsule with infiltration of adjacent thyroid parenchyma
-larger lesions with foci of hemorrhage and necrosis

Histological:
polygonal to spindle shaped cells forming nests, trabeculae and follicles
AMYLOID deposits from calcitonin

42
Q

Medullary carcinoma clinical course

A
  • May be mass or asymptomatic
  • may present with paraneoplastic syndrome VIP (diarrhea) and ACTH (cushing)
  • MEN2B more aggressive
  • hypocalcemia not prominent despite calcitonin

Treatment
total thyroidectomy
MEN-3 with RET mutation are offered prophylactic thyroidectomy as early as possible

43
Q

Anaplastic carcinoma

A

undifferentiated tumors accounting for 5%
65 years old
mortality approaches 100% with most patients dying in less than 1 year

histology: highly anaplastic cells, spindles, giant cells
- foci or papillary differentiation may suggest their origin from better differentiated tumor

Clinically:
presents as rapidly enlarging bulky mass
-usually spread
-dyspnea, dysphagia, hoarseness and cough de to compression of neck structures

no effective therapy

Genetic: inactivation of p53 or activating mutations of beta catenin

44
Q

Thyroglossal duct/cyst

A

incomplete atrophy o f the duct

  • midline cyst or anterior mass
  • lined by benign epithelium with normal thyroid and lymphocytes in the wall
  • infection with risk of abscess formation

MHD (81 decks)

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